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Stenting is also a treatment option. It can be performed without an abdominal incision by
introducing the catheters through arteries in the groin. However, not all patients with AAAs are
candidates for this treatment.
Regular physical examination and ultrasound checks are necessary to detect enlargement,
which may forewarn rupture. Large aneurysms or those that produce symptoms pose a
significant risk of rupture and necessitate immediate repair. In patients with poor distal runoff,
external grafting may be done.
Risk factor modification is fundamental in the medical management of abdominal aneurysm,
including control of hypocholesterolemia and hypertension. BBs are commonly prescribed to
reduce the risk of aneurysm expansion and rupture.
Special Considerations
Abdominal aneurysm requires meticulous preoperative and postoperative care, psychological
support, and comprehensive patient teaching. Following diagnosis, if rupture isn’t imminent,
elective surgery allows time for additional preoperative tests to evaluate the patient’s clinical
status.
Monitor vital signs, and type and crossmatch blood.
Use only gentle abdominal palpation.
As ordered, obtain renal function tests (BUN, creatinine, and electrolyte levels), blood
samples (complete blood count with differential), electrocardiogram and cardiac evaluation,
baseline pulmonary function tests, and ABG analysis.
Be alert for signs of rupture, which may be immediately fatal. Watch closely for signs of
acute blood loss (decreasing blood pressure; increasing pulse and respiratory rate; cool,
clammy skin; restlessness; and decreased sensorium).
If rupture does occur, the first priority is to get the patient to surgery immediately. Surgery
allows direct compression of the aorta to control hemorrhage. Large amounts of blood may be
needed during the resuscitative period to replace blood loss. In such a patient, renal failure
caused by ischemia is a major postoperative complication, possibly requiring hemodialysis.
Before elective surgery, weigh the patient, insert an indwelling urinary catheter and an I.V.
line, and assist with insertion of an arterial line and pulmonary artery catheter to monitor fluid
and hemodynamic balance. Give prophylactic antibiotics as ordered.
Explain the surgical procedure and the expected postoperative care in the ICU for patients
undergoing complex abdominal surgery (I.V. lines, ET and NG intubation, and mechanical
ventilation).
After surgery, in the ICU, closely monitor vital signs, intake and hourly output, neurologic
status (LOC, pupil size, and sensation in arms and legs), and ABG values. Assess the depth,
rate, and character of respirations and breath sounds at least every hour.
Watch for signs of bleeding (increased pulse and respiratory rates and hypotension) and back
pain, which may indicate that the graft is tearing. Check abdominal dressings for excessive
bleeding or drainage. Be alert for temperature elevations and other signs of infection. After
NG intubation for intestinal decompression, irrigate the tube frequently to ensure patency.
Record the amount and type of drainage.
Suction the ET tube often. If the patient can breathe unassisted and has good breath sounds
and adequate ABG values, tidal volume, and vital capacity 24 hours after surgery, it is likely
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he or she will be extubated and will require oxygen by mask.
Weigh the patient daily to evaluate fluid balance.
Help the patient walk as soon as able (generally the second day after surgery).
Provide psychological support for the patient and family. Help ease their fears about the ICU,
the threat of impending rupture, and surgery by providing appropriate explanations and
answering all questions.
FEMORAL AND POPLITEAL ANEURYSMS
Causes and Incidence
Femoral and popliteal aneurysms (sometimes called peripheral arterial aneurysms) are the end
result of progressive atherosclerotic changes occurring in the walls (medial layer) of these major
peripheral arteries. These aneurysmal formations may be fusiform (spindle-shaped) or saccular
(pouchlike); the fusiform type is three times more common. They may be singular or multiple
segmental lesions, often affecting both legs, and may accompany other arterial aneurysms
located in the abdominal aorta or iliac arteries.
Femoral and popliteal aneurysms are usually secondary to atherosclerosis. Rarely, they result
from congenital weakness in the arterial wall. They may also result from trauma (blunt or
penetrating), bacterial infection, or peripheral vascular reconstructive surgery (which causes
“suture line” aneurysms, or false aneurysms, in which a blood clot forms a second lumen).
This condition occurs most frequently in men older than 50. The clinical course is usually
progressive, eventually ending in thrombosis, embolization, and gangrene. Elective surgery
before complications arise greatly improves the prognosis.
Pathophysiology
As with other aneurysms, a weakening of the vessel wall caused by inflammation, proteolysis,
and changes in the matrix result in the outpouching seen in this condition.
Complications
Amputation of thrombosis
Emboli
Gangrene
Signs and Symptoms
Popliteal aneurysms may cause pain in the popliteal space when they’re large enough to
compress the medial popliteal nerve and edema and venous distention if the vein is compressed.
Femoral and popliteal aneurysms can produce symptoms of severe ischemia in the leg or foot
due to acute thrombosis within the aneurysmal sac, embolization of mural thrombus fragments
and, rarely, rupture. Symptoms of acute aneurysmal thrombosis include severe pain, loss of pulse
and color, coldness in the affected leg or foot, and gangrene. Distal petechial hemorrhages may
develop from aneurysmal emboli.
Diagnosis
Diagnosis is usually confirmed by bilateral palpation that reveals a pulsating mass above or
below the inguinal ligament in femoral aneurysm. When thrombosis has occurred, palpation
detects a firm, nonpulsating mass. Arteriography or ultrasound may be indicated in doubtful
situations. Arteriography may also detect associated aneurysms, especially those in the
abdominal aorta and the iliac arteries. Ultrasound may be helpful in determining the size of the
popliteal or femoral artery.
Treatment
Femoral and popliteal aneurysms require surgical bypass and reconstruction of the artery, usually
with an autogenous saphenous vein graft replacement. Arterial occlusion that causes severe
ischemia and gangrene may require leg amputation.
Special Considerations
Before corrective surgery:
Assess and record circulatory status, noting the location and quality of peripheral pulses in the
affected arm or leg.
Administer prophylactic antibiotics or anticoagulants, as ordered.
Discuss postoperative procedures and review the explanation of the surgery.
After arterial surgery:
Monitor carefully for early signs of thrombosis or graft occlusion (loss of pulse, decreased
skin temperature and sensation, and severe pain) and infection (fever).
Palpate distal pulses at least every hour for the first 24 hours and then as frequently as
ordered. Correlate these findings with preoperative circulatory assessment. Mark the sites on
the patient’s skin where pulses are palpable to facilitate repeated checks.
Help the patient walk soon after surgery to prevent venostasis and possible thrombus
formation.
To prepare the patient for discharge:
Tell the patient to immediately report any recurrence of symptoms because the saphenous
vein graft replacement can fail or another aneurysm may develop.
Explain to the patient with popliteal artery resection that swelling may persist for some time.
If antiembolism stockings are ordered, make sure they fit properly and teach the patient how
to apply them. Warn against wearing constrictive apparel.
If the patient is receiving anticoagulants, suggest measures to prevent bleeding, such as using
an electric razor. Tell the patient to report any signs of bleeding (bleeding gums, tarry stools,
and easy bruising) immediately. Explain the importance of follow-up blood studies to monitor
anticoagulant therapy. Warn the patient to avoid trauma, tobacco, and aspirin.
THROMBOPHLEBITIS
Causes and Incidence
An acute condition characterized by inflammation and thrombus formation, thrombophlebitis
may occur in deep (intermuscular or intramuscular) or superficial (subcutaneous) veins. DVT or
thrombophlebitis affects small veins, such as the soleal venous sinuses, or large veins, such as
the vena cava and the femoral, iliac, and subclavian veins, causing venous insufficiency. (See
Chronic venous insufficiency, page 78.) This disorder is typically progressive, leading to
pulmonary embolism, a potentially lethal complication. Superficial thrombophlebitis is usually
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self-limiting and seldom leads to pulmonary embolism. Thrombophlebitis often begins with
localized inflammation alone (phlebitis), but such inflammation rapidly provokes thrombus
formation. Rarely, venous thrombosis develops without associated inflammation of the vein
(phlebothrombosis).
Chronic Venous Insufficiency
Chronic venous insufficiency results from the valvular destruction of deep vein
thrombophlebitis, usually in the iliac and femoral veins, and occasionally the saphenous
veins. It’s often accompanied by incompetence of the communicating veins at the ankle,
causing increased venous pressure and fluid migration into the interstitial tissue. Clinical
effects include chronic swelling of the affected leg from edema, leading to tissue fibrosis, and
induration; skin discoloration from extravasation of blood in subcutaneous tissue; and stasis
ulcers around the ankle.
Treatment of small ulcers includes bed rest, elevation of the legs, warm soaks, and
antimicrobial therapy for infection. Treatment to counteract increased venous pressure, the
result of reflux from the deep venous system to surface veins, may include compression
dressings, such as a sponge rubber pressure dressing or a zinc gelatin boot (Unna boot). This
therapy begins after massive swelling subsides with leg elevation and bed rest.
Large stasis ulcers unresponsive to conservative treatment may require excision and skin
grafting. Patient care includes daily inspection to assess healing. Other care measures are the
same as for varicose veins.
DVT may be idiopathic, but it usually results from endothelial damage, accelerated blood
clotting, and reduced blood flow, known as the Virchow triad. Predisposing factors are
prolonged bed rest, trauma, surgery, childbirth, and use of hormonal contraceptives such as
estrogens. It occurs in about 80 of every 100,000 people; 1 of every 20 persons is affected at
some point during their lifetime. Males are at slightly greater risk than females. People older than
40 are also at increased risk.
Causes of superficial thrombophlebitis include trauma, infection, I.V. drug abuse, and
chemical irritation due to extensive use of the I.V. route for medications and diagnostic tests.
Pathophysiology
A thrombus occurs when an alteration in the epithelial lining causes platelet aggregation and
consequent fibrin entrapment of red and white blood cells and additional platelets. Thrombus
formation is more rapid in areas where blood flow is slower, due to greater contact between
platelet and thrombin accumulation. The rapidly expanding thrombus initiates a chemical
inflammatory process in the vessel epithelium, which leads to fibrosis. The enlarging clot may
occlude the vessel lumen partially or totally, or it may detach and embolize to lodge elsewhere in
the systemic circulation.
Complications
Pulmonary embolism
Chronic venous insufficiency
Signs and Symptoms
In both types of thrombophlebitis, clinical features vary with the site and length of the affected
vein. Although DVT may occur asymptomatically, it may also produce severe pain, fever, chills,
malaise and, possibly, swelling and cyanosis of the affected arm or leg. Superficial
thrombophlebitis produces visible and palpable signs, such as heat, pain, swelling, rubor,
tenderness, and induration along the length of the affected vein. Varicose veins may also be
present. (See Varicose veins, page 79.) Extensive vein involvement may cause lymphadenitis.
Varicose Veins
Varicose veins are dilated, tortuous veins, usually affecting the subcutaneous leg veins—the
saphenous veins and their branches. They can result from congenital weakness of the valves
or venous wall, diseases of the venous system such as deep vein thrombophlebitis, conditions
that produce prolonged venostasis such as pregnancy, or occupations that necessitate
standing for an extended period.
Varicose veins may be asymptomatic or may produce mild to severe leg symptoms,
including a feeling of heaviness; cramps at night; diffuse, dull aching after prolonged
standing or walking; aching during menses; fatigability; palpable nodules, and, with deep
vein incompetency, orthostatic edema and stasis pigmentation of the calves and ankles.
Treatment
In mild-to-moderate varicose veins, antiembolism stockings or elastic bandages counteract
pedal and ankle swelling by supporting the veins and improving circulation. An exercise
program such as walking promotes muscular contraction and forces blood through the veins,
thereby minimizing venous pooling. Severe varicose veins may necessitate stripping and
ligation or, as an alternative to surgery, injection of a sclerosing agent into small affected
vein segments.
To promote comfort and minimize worsening of varicosities:
Discourage the patient from wearing constrictive clothing.
Advise the patient to elevate the legs above heart level whenever possible and to avoid
prolonged standing or sitting.
After stripping and ligation or after injection of a sclerosing agent:
To relieve pain, administer analgesics as ordered.
Frequently check circulation in toes (color and temperature) and observe elastic bandages
for bleeding. When ordered, rewrap bandages at least once a shift, wrapping from toe to
thigh, with the leg elevated.
Watch for signs of complications, such as sensory loss in the leg (which could indicate
saphenous nerve damage), calf pain (thrombophlebitis), and fever (infection).
Diagnosis
Findings are usually nonspecific and are not reliable for making the diagnosis of DVT. Essential
laboratory tests include:
Duplex Doppler is most commonly performed; this makes it possible to noninvasively
examine the major veins (but not calf veins).
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CONFIRMING DIAGNOSIS Compression ultrasonography with Doppler is the diagnostic test of
choice in the evaluation of DVT.
Diagnosis must also rule out PAD, lymphangitis, cellulitis, and myositis.
Diagnosis of superficial thrombophlebitis is based on physical examination (redness and
warmth over the affected area, palpable vein, and pain during palpation or compression).
Treatment
The goals of treatment are to control thrombus development, prevent complications, relieve pain,
and prevent recurrence of the disorder. Symptomatic measures include bed rest, with elevation of
the affected arm or leg; warm, moist soaks to the affected area; and analgesics. After the acute
episode of DVT subsides, the patient may resume activity while wearing antiembolism stockings
that were applied before getting out of bed.
Treatment also includes anticoagulants to prolong clotting time. While warfarin is still an
option for the treatment of DVT, new medications are now available that are safer, as effective,
and do not require monitoring of blood levels through frequent lab draws. These medications are
called direct factor Xa inhibitors and include rivaroxaban and apixaban. If the patient is not a
candidate for these novel medications, low-molecular-weight (LMW) heparin has been shown to
be effective in treating DVT or can be used as bridge therapy until a therapeutic level of warfarin
is achieved. Although LMW heparin is more expensive, it doesn’t require monitoring for its
anticoagulant effect, either. Full anticoagulant doses must be discontinued during any operative
period because of the risk of hemorrhage. After some types of surgery, especially major
abdominal or pelvic operations, prophylactic doses of anticoagulants may reduce the risk of DVT
and pulmonary embolism. For lysis of acute, extensive DVT, treatment may include
thrombolysis with or without thrombectomy. Rarely, DVT may cause complete venous
occlusion, which necessitates venous interruption through simple ligation to vein plication, or
clipping. Embolectomy and insertion of a vena caval umbrella or filter may also be done.
Therapy for severe superficial thrombophlebitis may include an anti-inflammatory drug such
as indomethacin, antiembolism stockings, warm soaks, and elevation of the leg.
Special Considerations
Patient teaching, identification of high-risk patients, and measures to prevent venostasis can
prevent DVT; close monitoring of anticoagulant therapy can prevent serious complications such
as internal hemorrhage.
Enforce bed rest as ordered, and elevate the patient’s affected arm or leg. If you plan to use
pillows for elevating the leg, place them so they support the entire length of the affected
extremity to prevent possible compression of the popliteal space.
Apply warm soaks to increase circulation to the affected area and to relieve pain and
inflammation. Give analgesics to relieve pain, as ordered.
Measure and record the affected arm or leg’s circumference daily, and compare this
measurement to the other arm or leg. To ensure accuracy and consistency of serial
measurements, mark the skin over the area and measure at the same spot daily.
Administer heparin I.V., as ordered, with an infusion monitor or pump to control the flow rate
if necessary. Remember that this medication is not being used as often with the growing
popularity of direct factor Xa inhibitors.
Measure partial thromboplastin time regularly for the patient on heparin therapy; prothrombin
time and international normalized ratio (INR) for the patient on warfarin (therapeutic
anticoagulation values are 1½ to 2 times control values for prothrombin time and an INR of 2
to 3). Watch for signs and symptoms of bleeding, such as dark, tarry stools; coffee-ground
vomitus; and ecchymosis. Encourage the patient to use an electric razor and to avoid
medications that contain aspirin.
Be alert for signs of pulmonary emboli (crackles, dyspnea, hemoptysis, sudden changes in
mental status, restlessness, and hypotension).
To prepare the patient with thrombophlebitis for discharge:
Emphasize the importance of follow-up blood studies to monitor anticoagulant therapy, if
necessary.
If the patient is being discharged on heparin therapy, teach the patient or family how to give
subcutaneous injections. If the patient requires further assistance, arrange for a home health
nurse.
Tell the patient to avoid prolonged sitting or standing to help prevent recurrence.
Teach the patient how to properly apply and use antiembolism stockings. Tell the patient to
report any complications such as cold, blue toes. (See Preventing thrombophlebitis.)
PREVENTION
PREVENTING THROMBOPHLEBITIS
To prevent thrombophlebitis in a high-risk patient, perform range-of-motion exercise
while the patient is on bed rest, use intermittent pneumatic calf massage during lengthy
surgical or diagnostic procedures, apply antiembolism stockings postoperatively, and
encourage early ambulation.
After some types of surgery, especially major abdominal or pelvic operations, prophylactic
doses of anticoagulants may reduce the risk of deep vein thrombosis and pulmonary
embolism.
RAYNAUD DISEASE
Causes and Incidence
Raynaud disease is one of several primary arteriospastic disorders characterized by episodic
vasospasm in the small peripheral arteries and arterioles, precipitated by exposure to cold or
stress. This condition occurs bilaterally and usually affects the hands or, less often, the feet.
Raynaud disease is most prevalent in females, particularly those between puberty and 40 years
old. It’s a benign condition, requiring no specific treatment and causing no serious sequelae.
Although the cause is unknown, several theories account for the reduced digital blood flow:
intrinsic vascular wall hyperactivity to cold, increased vasomotor tone due to sympathetic
stimulation, and antigen–antibody immune response (the most likely theory because abnormal
immunologic test results accompany Raynaud phenomenon). Risk factors include associated
diseases (Buerger disease, atherosclerosis, rheumatoid arthritis, scleroderma, and SLE) and
smoking.
This disorder affects females more often than males.
Raynaud phenomenon, however, a condition commonly associated with several connective
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tissue disorders—such as scleroderma, SLE, or polymyositis—has a progressive course, leading
to ischemia, gangrene, and amputation. Distinguishing between the two disorders is difficult
because some patients who experience mild symptoms of Raynaud disease for several years may
later develop overt connective tissue disease—especially scleroderma.
Pathophysiology
Complications
Ischemia
Gangrene
Amputation
Signs and Symptoms
After exposure to cold or stress, the skin on the fingers typically blanches and then becomes
cyanotic before changing to red and before changing from cold to normal temperature.
Numbness and tingling may also occur. These symptoms are relieved by warmth. In longstanding disease, trophic changes, such as sclerodactyly, ulcerations, or chronic paronychia, may
result. Although it’s extremely uncommon, minimal cutaneous gangrene necessitates amputation
of one or more phalanges.
Diagnosis
Clinical criteria that establish Raynaud disease include skin color changes induced by cold or
stress; bilateral involvement; absence of gangrene or, if present, minimal cutaneous gangrene;
normal arterial pulses; and patient history of clinical symptoms of longer than 2 years’ duration.
Diagnosis must also rule out secondary disease processes, such as chronic arterial occlusive or
connective tissue disease.
Treatment
Initially, treatment consists of avoidance of cold, mechanical, or chemical injury; cessation of
smoking; and reassurance that symptoms are benign. Because adverse drug effects, especially
from vasodilators, may be more bothersome than the disease itself, drug therapy is reserved for
unusually severe symptoms. Such therapy may include low doses of nifedipine. Sympathectomy
may be helpful when conservative modalities fail to prevent ischemic ulcers and becomes
necessary in less than 25% of patients.
Special Considerations
Warn the patient against exposure to the cold. Tell the patient to wear mittens or gloves in
cold weather or when handling cold items or defrosting the freezer.
Advise the patient to avoid stressful situations and to stop smoking.
Instruct the patient to inspect the skin frequently and to seek immediate care for signs of skin
breakdown or infection.
Teach the patient about drugs, their use, and their adverse effects.
Provide psychological support and reassurance to allay the patient’s fear of amputation and
disfigurement.
BUERGER DISEASE
Causes and Incidence
Buerger disease (sometimes called thromboangiitis obliterans)—an inflammatory,
nonatheromatous occlusive condition—causes segmental lesions and subsequent thrombus
formation in the small and medium arteries (and sometimes the veins), resulting in decreased
blood flow to the feet and legs. This disorder may produce ulceration and, eventually, gangrene.
Buerger disease is caused by vasculitis, an inflammation of blood vessels, primarily of the
hands and feet. The vessels become constricted or totally blocked, reducing blood flow to the
tissues and resulting in pain and, eventually, damage.
This disorder occurs in 12 to 20 of every 100,000 people. Incidence is highest among males 20
to 40 years old who have a history of smoking or chewing tobacco. It may be associated with a
history of Raynaud disease and may occur in people with autoimmune disease.
Pathophysiology
The pathophysiology of Buerger disease is not well understood. In the acute phase, occlusive
thrombi develop in arteries and veins of distal extremities. Next, thrombi start to organize into
larger vessels. Over time, inflammation resides but fibrosis and organized thrombi remain.
There is also evidence that dysfunction of the endothelial layer of the vessels occurs, as well
as the possibility of issues with prothrombin.
Complications
Gangrene
Muscle atrophy
Ulceration
Signs and Symptoms
Buerger disease typically produces intermittent claudication of the instep, which is aggravated by
exercise and relieved by rest. During exposure to low temperature, the feet initially become cold,
cyanotic, and numb; later, they redden, become hot, and tingle. Occasionally, Buerger disease
also affects the hands, possibly resulting in painful fingertip ulcerations. Associated signs and
symptoms may include impaired peripheral pulses, migratory superficial thrombophlebitis and,
in later stages, ulceration, muscle atrophy, and gangrene.
Diagnosis
Patient history and physical examination strongly suggest Buerger disease. Supportive diagnostic
tests include:
Doppler ultrasonography to show diminished circulation in the peripheral vessels
angiography or arteriography to locate lesions and rule out atherosclerosis.
Treatment
The primary goals of treatment are to relieve symptoms and prevent complications. Such therapy
may include an exercise program that uses gravity to fill and drain the blood vessels or, in severe
disease, a lumbar sympathectomy to increase blood supply to the skin. Aspirin and vasodilators
may also be used. Amputation may be necessary for nonhealing ulcers, intractable pain, or
gangrene.
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Special Considerations
Strongly urge the patient to stop smoking to enhance the treatment’s effectiveness. Symptoms
may disappear if the patient stops tobacco use. If necessary, refer the patient to a self-help
group to stop smoking.
Warn the patient to avoid precipitating factors, such as emotional stress, exposure to extreme
temperatures, and trauma.
Teach the patient proper foot care, especially the importance of wearing well-fitting shoes and
cotton or wool socks. Show the patient how to inspect feet daily for cuts, abrasions, and signs
of skin breakdown, such as redness and soreness. Remind the patient to seek medical attention
at once after any trauma.
If the patient has ulcers and gangrene, enforce bed rest and use a padded footboard or bed
cradle to prevent pressure from bed linens. Protect the feet with soft padding. Wash them
gently with a mild soap and tepid water, rinse thoroughly, and pat dry with a soft towel.
Provide emotional support. If necessary, refer the patient for psychological counseling to help
the patient cope with restrictions imposed by this chronic disease. If the patient has undergone
amputation, assess rehabilitative needs, especially regarding changes in body image. Refer the
patient to physical therapists, occupational therapists, and social service agencies, as needed.
PERIPHERAL ARTERY DISEASE
Causes and Incidence
PAD, referred to as arterial occlusive disease, is the obstruction or narrowing of the lumen of the
aorta and its major branches, causing an interruption of blood flow, usually to the legs and feet.
PAD may affect the carotid, vertebral, innominate, subclavian, mesenteric, and celiac arteries.
Occlusions may be acute or chronic and commonly cause severe ischemia, skin ulceration, and
gangrene.
The prognosis depends on the occlusion’s location, the development of collateral circulation to
counteract reduced blood flow, and, in acute disease, the time elapsed between occlusion and its
removal.
Predisposing factors include smoking; aging; such conditions as hypertension, hyperlipidemia,
and diabetes; and a family history of vascular disorders, MI, or stroke. PAD has no racial
predilection. Men older than 50 are at increased risk for intermittent claudication, a common sign
of PAD.
Pathophysiology
PAD is a common complication of atherosclerosis. The occlusive mechanism may be
endogenous, due to emboli formation or thrombosis, or exogenous, due to trauma or fracture.
Complications
Severe ischemia
Skin ulceration
Gangrene
Limb loss
Signs and Symptoms
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